Basic Research
Copyright ©2006 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Jul 21, 2006; 12(27): 4331-4337
Published online Jul 21, 2006. doi: 10.3748/wjg.v12.i27.4331
Cortex cinnamomi extract prevents streptozotocin- and cytokine-induced β-cell damage by inhibiting NF-κB
Kang-Beom Kwon, Eun-Kyung Kim, Eun-Sil Jeong, Young-Hoon Lee, Young-Rae Lee, Jin-Woo Park, Do-Gon Ryu, Byung-Hyun Park
Kang-Beom Kwon, Eun-Kyung Kim, Eun-Sil Jeong, Do-Gon Ryu, Department of Physiology, School of Oriental Medicine, Wonkwang University, Iksan 570-749, South Korea
Young-Hoon Lee, Department of Oral Anatomy, School of Dentistry, Chonbuk National University, Jeonju 561-756, Jeonbuk, South Korea
Young-Rae Lee, Jin-Woo Park, Byung-Hyun Park, Department of Biochemistry, Medical School, Institute for Healthcare Technology Development, Medical Research Center, Chonbuk National University, Jeonju 561-756, Jeonbuk, South Korea
Supported by the Regional Research Center Program of the Korean Ministry of Education & Human Resources Development through the Center for Healthcare Technology Development
Correspondence to: Byung-Hyun Park, Department of Biochemistry, Medical School, Institute for Healthcare Technology Development, Medical Research Center, Chonbuk National University, Jeonju 561-756, Jeonbuk, South Korea. bhpark@chonbuk.ac.kr
Telephone: +82-63-2703139 Fax: +82-63-2749833
Received: March 7, 2006
Revised: March 8, 2006
Accepted: March 27, 2006
Published online: July 21, 2006
Abstract

AIM: To clarify the mechanism underlying the anti-diabetic activities of cortex cinnamomi extract (CCE).

METHODS: To induce in vivo diabetes, mice were injected with streptozotocin (STZ) via a tail vein (100 mg STZ/kg body weight). To determine the effects of CCE, mice were administered CCE twice daily for 7 d by oral gavage starting 1 wk before the STZ injection. Blood glucose and plasma insulin concentration were measured as an index of diabetes. Also, to induce cytotoxicity of RINm5F cells, we treated with cytokines (IL-1β (2.0 ng/mL) and IFN-γ (100 U/mL)). Cell viability and nitric oxide production were measured colorimetrically. Inducible nitric oxide synthase (iNOS) mRNA and protein expression were determined by RT-PCR and Western blotting, respectively. The activation of NF-κB was assayed by using gel mobility shift assays of nuclear extracts.

RESULTS: Treatment of mice with STZ resulted in hyperglycemia and hypoinsulinemia, which was further evidenced by immunohistochemical staining of islets. However, the diabetogenic effects of STZ were completely prevented when mice were pretreated with CCE. The inhibitory effect of CCE on STZ-induced hyperglycemia was mediated through the suppression of iNOS expression. In rat insulinoma RINm5F cells, CCE completely protected against interleukin-1β and interferon-γ-mediated cytotoxicity. Moreover, RINm5F cells incubated with CCE showed significant reductions in interleukin-1β and interferon-γ-induced nitric oxide production and in iNOS mRNA and protein expression, and these findings correlated well with in vivo observations.

CONCLUSION: The molecular mechanism by which CCE inhibits iNOS gene expression appears to involve the inhibition of NF-κB activation. These results reveal the possible therapeutic value of CCE for the prevention of diabetes mellitus progression.

Keywords: Cortex cinnamomi; Diabetes; Streptozotocin; Cytokine; NF-κB